POS0927 COMBINED BRAIN/HEART MAGNETIC RESONANCE IMAGING REVEALS SUBCLINICAL BRAIN LESIONS IN PATIENTS WITH INFLAMMATORY ARTHRITIDES AND CARDIAC SYMPTOMS
Authors: G. Markousis-Mavrogenis, A. I. Venetsanopoulou, A. Pieta, I. Ntalas, C. Naka, I. Pagounis, D. Toliopoulos, G. Mouka, P. Voulgari, S. I. Mavrogeni
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Inflammatory arthritides (IA) can affect diverse body tissues beyond joints, including the heart [1,2]. Particularly in chronic inflammatory states, circulating immune mediators can also induce central nervous system inflammation [3]. Nevertheless, little is currently known about the consequences of cardiac inflammation on the occurrence of brain lesions in these patients. <h3>Objectives</h3> We hypothesized that patients with IA and cardiac symptoms would show evidence of brain lesions, and that the presence of cardiac inflammation would be associated with the presence of brain lesions. We thus investigated patients with IA and compared them to a cohort of disease-controls using combined brain/heart magnetic resonance imaging (MRI). <h3>Methods</h3> Patients with IA and shortness of breath, chest pain and/or palpitations (n=25) were compared to age-matched disease-controls with non-autoimmune cardiovascular disease (CVD) (n=30) using a 1.5T MRI system. The presence of white matter hyperintensities (WMHs) was investigated in subcortical/deep/periventricular white matter, the basal ganglia, pons, brainstem, or mesial temporal lobe. Cardiac function and inflammation were investigated using standard protocols. Patients with IA were diagnosed with rheumatoid arthritis [14 (56%)], ankylosing spondylitis [5 (20%)], juvenile rheumatoid arthritis [3 (12%)], mixed connective tissue disease [2 (8%)] or enteropathic arthritis [1 (4%)]. Disease controls had various CVDs including coronary artery disease [5 (17%)], myocarditis [5 (17%)], hypertension [3 (10%)], Duchenne muscular dystrophy [3 (10%)], and others. <h3>Results</h3> Patients with IA and disease-controls respectively had a median (IQR) age of 45 (39, 51) vs. 53 (40, 57) years (p=0.269), and 16 (64%) vs. 7 (23%) were women (p=0.002). WMHs were detected in ≥1 brain area in 15 (60%) patients with IA and 15 (54%) disease-controls (p=0.620). The majority of participants had WMHs in subcortical [29 (53%)], periventricular [5 (9%)], or deep WM [11 (20%)]. Some also had cortical lesions [5 (9%)], while basal nuclear, brainstem and mesial temporal lesions were rare [1 (2%) for all]. Amongst subjects with WMHs, the median (IQR) number of brain lesions in patients with IA and disease-controls was 1 (1, 2) for both groups (p=0.635). There were no significant differences in the distribution of brain lesions between groups. Amongst patients with IA, each 0.1-unit increase in cardiac T2-ratio was associated with an increased probability of WMH occurrence [odds ratio (95%): 1.29 (1.05-1.59), p=0.016] and higher cardiac T2-ratio (per 0.1-unit change) and extracellular volume fraction (ECV) were associated with a higher WMH lesion burden in linear regression analysis [Beta (95% confidence interval): 0.08 (0.01-0.15), p=0.021 and 0.22 (0.03-0.41), p=0.027, respectively]. MRI-derived left/right-ventricular ejection fraction, early/late-gadolinium enhancement and T1/T2 mapping were not associated with the presence of WMHs. <h3>Conclusion</h3> In patients with IA and cardiac symptoms, 60% showed evidence of subclinical brain lesions, which was on average as prevalent as in age-matched disease-controls with non-autoimmune CVD. Higher myocardial T2-ratio, an MRI-derived surrogate of myocardial edema, was associated with the presence of WMHs, and higher T2-ratio as well as myocardial ECV values were predictive of higher WMH burden. Further research is required to determine the clinical relevance of these findings. <h3>References</h3> [1]Venetsanopoulou AI, et al. Rheumatol Int. 2020;40(8):1181-1191. doi:10.1007/s00296-020-04616-2 [2]Markousis-Mavrogenis G, et al. J Clin Med. 2022;11(5):1428. doi:10.3390/jcm11051428 [3]Sun Y, et al. Front Aging Neurosci. 2022;14:903455. doi:10.3389/fnagi.2022.903455 <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.